ArticleThe Journal of clinical investigation1991
Skeletal actin mRNA increases in the human heart during ontogenic development and is the major isoform of control and failing adult hearts.
Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 125 citations in OpenAlex.
- Perinatal death in pig models of hypertrophic cardiomyopathy carrying sarcomere pathogenic variants.Journal of molecular and cellular cardiology plus · 2025Article
- Cardiac maturation.Journal of molecular and cellular cardiology · 2024Review
- Cardiac foetal reprogramming: a tool to exploit novel treatment targets for the failing heart.Journal of internal medicine · 2020Review
- Human pluripotent stem cell-derived cardiomyocytes as a target platform for paracrine protection by cardiac mesenchymal stromal cells.Scientific reports · 2020Article
- Sarcomeric Gene Variants and Their Role with Left Ventricular Dysfunction in Background of Coronary Artery Disease.Biomolecules · 2020Review
- Heart Failure in Pediatric Patients With Congenital Heart Disease.Circulation research · 2017Review
- A gain-of-function ACTC1 3'UTR mutation that introduces a miR-139-5p target site may be associated with a dominant familial atrial septal defect.Scientific reports · 2016Article
- Effective top-down LC/MS+ method for assessing actin isoforms as a potential cardiac disease marker.Analytical chemistry · 2015Article
- Harnessing fetal and adult genetic reprograming for therapy of heart disease.Journal of nature and science · 2015Article
- Modelling sarcomeric cardiomyopathies in the dish: from human heart samples to iPSC cardiomyocytes.Cardiovascular research · 2015Review
- Sarcomeric protein isoform transitions in cardiac muscle: a journey to heart failure.Biochimica et biophysica acta · 2015Review
- The W-loop of alpha-cardiac actin is critical for heart function and endocardial cushion morphogenesis in zebrafish.Molecular and cellular biology · 2012Article
- β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.Circulation research · 2011Article
- EST-based identification of genes expressed in skeletal muscle of the mandarin fish (Siniperca chuatsi).Genomics, proteomics & bioinformatics · 2011Article
- Investigation of changes in skeletal muscle alpha-actin expression in normal and pathological human and mouse hearts.Journal of muscle research and cell motility · 2010Article
- Re-expression of alpha skeletal actin as a marker for dedifferentiation in cardiac pathologies.Journal of cellular and molecular medicine · 2009Article
- Cardiogenic differentiation and transdifferentiation of progenitor cells.Circulation research · 2008Review
- Myofibrillar remodeling in cardiac hypertrophy, heart failure and cardiomyopathies.The Canadian journal of cardiology · 2006Review
- Thin filament remodeling in failing myocardium.Heart failure reviews · 2005Review
- The slow skeletal muscle troponin T gene is expressed in developing and diseased human heart.Molecular and cellular biochemistry · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the two sarcomeric actins, alpha-skeletal and alpha-cardiac, is regulated in the rodent heart in response to developmental, hormonal, and hemodynamic stimuli. Little is known in man, except that both isogenes were found to be coexpressed in three adult ventricles. In this report, we investigated the isoactin mRNA composition in ventricles from 21 control patients (4 fetal, 5 juvenile, 12 adult) and from 15 patients undergoing cardiac transplantation (5 idiopathic dilated cardiomyopathies, 5 ischemic myopathies with myocardial infarcts, 5 diverse etiologies) by two different and complementary techniques: RNA dot blot analysis with specific cDNA probes, and primer extensions with an oligonucleotide common to alpha-cardiac and alpha-skeletal actins. In the case of dot blot analysis, quantification of each isoform was performed by using as standards RNA transcripts obtained from cloned human alpha-actin sequences, and the total amount of sarcomeric actin mRNA was evaluated as a function of total poly(A+)RNA. We found that both isogenes are always coexpressed, and that the isoactin pattern changes during development. In utero and in neonatal hearts, alpha-skeletal actin mRNA represents less than or equal to 20% of sarcomeric actins, it increases to 48 +/- 6% during the first decade after birth and becomes the predominant isoform of adult hearts (60.4 +/- 8.5%). The 15 adult failing hearts exhibited the same isoactin pattern as the control ones (62.84 +/- 11.06%), and there was no difference in expression between patients with dilated cardiomyopathy or ischemic heart disease. These observations demonstrate that cardiac development in man, in contrast to rodent heart, is characterized by an up-regulation of the skeletal actin gene, the expression of which does not change in hypertrophied and failing hearts, and suggest that the actin and myosin heavy chain families are independently regulated in human heart.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.